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P Raynier

Publications and source records attributed to P Raynier.

10 recordsLinked to original sources
PubMed1990

[Left intraventricular flow during isovolumic relaxation. Frequency, significance, mechanism].

Supplementary intraventricular flow during the left ventricular isovolumic relaxation period "isovolumic relaxation flow", was described for the first time in 1987 by Sasson. This flow was searched for in 13 patients with hypertrophic obstructive cardiomyopathy (HOCM), 58 patients with aortic valve stenosis (AVS) and 41 normal control patients. It was detected in 77% of patients with HOCM, 50% of patients with AVS and 5% of normal controls. The flow was usually recorded throughout the isovolumic relaxation period and lasted an average 104 ms (range 70 to 140 ms) with a velocity of 0.74 m/s (range 0.25 to 1.70 m/s). It was detected along the middle third of the interventricular septum, directed towards the cardiac apex, coded in red in colour Doppler studies. The other Doppler echocardiographic signs associated with isovolumic relaxation flow were: small left ventricular chambers, normo- or hyperkinetic wall motion, systolic apical cavity obliteration, intraventricular systolic acceleration with a left systolic peak (74% of cases) but with no correlation between the velocity of this flow and that of isovolumic relaxation flow. Isovolumic relaxation flow results from an intraventricular pressure gradient related to asynchronous relaxation and the resulting redistribution of blood in the left ventricle. It would seem to be a marker of hyperkinetic wall motion together with systolic apical cavity obliteration and the resulting intraventricular systolic accelerated flow. It should not be confused with the mitral E wave, especially in patients with atrial fibrillation.

Adult↗
PubMed1990

[Critical analysis of the response to antihypertensive therapy. Report of 102 cases].

UNLABELLED: One hundred and two patients with mild to moderate hypertension, non responding to a placebo therapy, were given an antihypertensive drug for a mean period of 6 weeks (range: 3-12 weeks). Their blood pressure (BP) was measured before and after active treatment by both a mercury manometer at the clinic and an ambulatory apparatus (Spacelabs 5200 or 90202). The clinic BP figures were poorly correlated with the 24 hour ambulatory BP levels, as well as the magnitude of decrease in clinic BP with the reduction in ambulatory BP. Twenty eight patients who were considered as "clinic responders" had in fact not significantly lowered their ambulatory DBP and, conversely, 16 patients were "clinic non responders" whereas they were "ambulatory responders". The patients were divided into 2 groups, according to White's and Morgan Roth's recommendations: group I (n = 61) with a percentage of pathological DBP readings (greater than 90 mmHg) during daytime as high as 50% or more, and group II (n = 41) with a percentage less than 50%. The correlations between the 2 methods of BP measurement were closer within the group I than within the group II and the rate of discrepancies between the "clinic" and "ambulatory responders" was lower. On the other hand, we identified the group II patients as being often "clinic responders" but rarely "ambulatory responders", whereas the inverse trend was observed in the group I. IN CONCLUSION: even in non placebo responding hypertensive patients the clinic BP measurement might be not sufficient for proper evaluation of an antihypertensive drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Blood pressure response to antihypertension treatment. Comparison of data obtained at the doctor's office and by ambulatory blood pressure measurement].

A comparative study of clinical and ambulatory responses to antihypertensive treatment was conducted retrospectively in 69 patients with mild to moderate arterial hypertension. The patients received different drugs, but blood pressure (BP) was measured by the same methods in each of them. (a) Clinical BP was measured with a mercury manometer some time after taking the last dose of antihypertensive drug: 24 hours in patients who took one daily dose, 12 hours in those who took two daily doses. (b) Ambulatory BP was measured with a Spacelabs SPM 5200 instrument over a minimum of 24 hours. The parameters compared were: (1) BP figures recorded. Correlation was very poor as regards both SBP (r = 0.42 before treatment, r = 0.55 after treatment) and DBP (r = 0.40 and r = 0.46 respectively). The mean BP value was lower in the ambulatory group than in the clinical group (-20/-12 mmHg), the difference being slightly less marked after treatment (-12/-6 mmHg). (2) Degree of absolute reduction of BP induced by treatment. Correlation was very poor between the two methods as regards both SBP (r = 0.46) and DBP (r = 0.49). (3) Proportion of responders and non-responders to treatment, the clinical response being defined as normalization and/or more than 10 p. 100 reduction of DBP, and the ambulatory response as a significant decrease of mean diastolic value over 24 hours. Among the 69 patients studied, there were 51 concordant cases (36 responders, 15 non-responders with the two methods) and 18 discordant cases (10 clinical responders but ambulatory non-responders, 8 clinical non-responders but ambulatory responders).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Left ventricular relaxation and ambulatory blood pressure in mild, untreated arterial hypertension].

Twenty patients with mild, untreated arterial hypertension had ambulatory blood pressure recordings and a digitized echocardiographic study of the left ventricle with measurement of its mass (LVM) and of relaxation parameters. A significant correlation was found between LVM and ambulatory systolic pressure during daytime (r = 0.64; p less than 0.01; n = 20) and during 24 hours (r = 0.79; p less than 0.001; n = 16). One of the relaxation parameters studied, the time taken to reach maximal speed of left ventricular enlargement, was closely related to the diurnal diastolic blood pressure (r = 0.58; p less than 0.01; n = 20), whereas in this population with mild arterial blood pressure none of the parameters was related to the amount of increase of LVM. One may therefore consider the abnormalities of left ventricular relaxation as likely to appear at an early stage of arterial hypertension; their discovery may antedate that of LVM and confirm that the hypertensive disease is real. However, the methodological problems encountered with type of exploration ought to be stressed: left ventricular relaxation is a multifactorial phenomenon, and its echocardiographic approach is subject to many hazards.

Adult↗
PubMed1988

[Left ventricular hypertrophy in hypertensive patients. Ultrasonic and physiopathology: therapeutic implications].

Hypertensive left ventricular hypertrophy can easily be diagnosed by echocardiography. It occurs in 30-50 per cent of hypertensive patients and has recently been shown to be a potent and independent predictor of morbidity and mortality, increasing the risk of sudden death, arrhythmia and severe coronary events. The condition usually presents as concentric left ventricular hypertrophy with symmetrically or asymmetrically thickened ventricular walls, but it may also be found with a dilated cavity. Its presence is a definite indication for active medical treatment. Guidelines for the choice of a particular antihypertensive drug are not yet available. Regression of the hypertrophy seems to be a rational goal of the treatment, but the beneficial effects of such a regression on left ventricular relaxation need further evaluation.

Cardiomegaly↗
PubMed1987

[Thrombopenia caused by pentosan polysulfate].

Two case-reports of thrombopenias induced by pentosane polysulfate (PSP) are reported. PSP may play a direct role in the genesis of the thrombopenia appearing between the 5th and 15th day of treatment, or a sensitizing role where the thrombopenia occurs quite rapidly following heparin treatment. The clinical complications are haematomas, arterial or venous thromboses and haemorrhages. The platelet aggregation test is always positive in the presence of PSP. The immunological origin is probable. Monitoring of the platelet count is recommanded with this treatment.

Aged↗